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C. Hirche et al.
clothing and any jewelry should be removed unless
it is merged with the patient (e.g., polyvinyl chloride, polyester). There are controversial discussions
about cooling of burns, especially regarding the correct time, temperature, timeframe, and medium.
Many patients are mistakenly cooled down and
arrive with mild to severe hypothermia. Cooling has
a high analgesic potency and can reduce area of the
zone of stasis where capillary perfusion is reduced
when applied correctly. If the burnt body surface
area is small (<10%), cooling of the burn should be
performed [19]. Medium-tempered running tap
water (approximately 15–20°C) with a maximum
cooling time of 15min is recommended, while specially manufactured burn dressings (Water−Gel®,
Burn−Pack®) have raised concerns regarding hypothermia following application due to handling
errors. Dressings are important for pain management and to prevent the burnt area from contamination as a potential source of infection and
inammation. Dressings also play a role in thermal
balance. Customary metal lms (e.g., Metalline®)
can reduce the risk of undercooling as a further
external measure with impact on burn progression
[20, 21].
Goal-directed, individual burn wound care
includes specialist treatments, regular antiseptic
dressing with appropriate wound climate, balanced uid supply to prevent unnecessary edema,
and analgesia in order to reduce pain-associated
vasoactive mediator release.
10.4.2 Secondary Necrosis
Although research is going on, current milestones
of treatment include adequate uid resuscitation,
nutritional support, and local wound care, with
focus on topical antimicrobial agents and dressings. With potential therapeutic application,
resolvins, a class of endogenous mediators
derived from omega-3 polyunsaturated fatty
acids, have been shown to regulate the resolution
of inammation in an animal model. By preserving the microvascular network, the agent was
shown to enhance neutrophil access to the dermis, but prevented neutrophil-mediated damage
[8].
Ipaktchi etal. hypothesized that topical attenuation of burn wound inammatory signaling
will control the dermal inammatory source,
attenuate SIRS, and reduce acute lung injury.
They applied a topical p38 mitogen-activated
protein kinase (MAPK) inhibitor to wounds.
Topical p38 MAPK inhibition resulted in signicantly less pulmonary inammatory response by
reducing pulmonary neutrophil sequestration,
pulmonary cytokine expression, and a signicant
reduction in pulmonary microvascular injury and
edema formation. They concluded that there is a
strong interaction between dermal inammation
and systemic inammatory response; thus, attenuating local inammatory signaling appears
effective in reducing SIRS and subsequent systemic complications after burn injury [22].
10.4.3 Tertiary Necrosis
In order to prevent tertiary necrosis, adequate
necrectomy remains the key factor in the preparation of high-rate transplant take. In addition, a
balanced specialist and multidisciplinary therapy
includes adequate uid supply, nutritional support, and local wound care. Vasoactive mediators
may lead to capillary occlusion impairing transplant take. If epithelial islands are surrounded by
tertiary necrosis, secondary wound healing vs.
retransplantation have to be evaluated on the
basis of affected burned area, localization, and
expected healing period. Hypertrophic scarring,
dyspigmentation, and potential contractures can
result from tertiary necrosis.
Key Messages for Necrosis in Burns
Primary necrosis:
Inammation, capillary leakage, edema,
hypercoagulability, venous thrombosis, and arteriole and capillary stasis lead to burn progression
and involve a number of factors which are linked.
Establish early diagnosis of primary necrosis
and debridement and adequate initial care.
Secondary necrosis:
Try to prevent or limit inammation.
Conversion zones may lead to secondary
necrosis.
10 Necrosis inBurns
85
Tertiary necrosis:
Sufcient necrectomy enables high rate of
transplant take.
Loss of transplant may lead to tertiary
necrosis.
Tertiary necrosis necessitates secondary heal-
ing or retransplantation.
References
1. Jackson DM. [The diagnosis of the depth of burning].
Br J Surg. 1953;40:588–96.
2. Jackson DM.Second thoughts on the burn wound. J
Trauma. 1969;9:839–62.
3. Shupp JW, Nasabzadeh TJ, Rosenthal DS, et al. A
review of the local pathophysiologic bases of burn
wound progression. J Burn Care Res. 2010;31:849–73.
4. Gravante G, Filingeri V, Delogu D, et al. Apoptotic
cell death in deep partial thickness burns by coexpression analysis of TUNEL and Fas. Surgery.
2006;139:854–5.
5. Shakespeare P.Burn wound healing and skin substitutes. Burns. 2001;27:517–22.
6. Singh V, Devgan L, Bhat S, Milner SM. The pathogenesis of burn wound conversion. Ann Plast Surg.
2007;59:109–15.
7. Kremer T, Harenberg P, Hernekamp F, et al. Highdose vitamin C treatment reduces capillary leakage
after burn plasma transfer in rats. J Burn Care Res.
2010;31:470–9.
8. Bohr S, Patel SJ, Sarin D, et al. Resolvin D2 prevents secondary thrombosis and necrosis in a
mouse burn wound model. Wound Repair Regen.
2012;21(1):35–43.
9. Gravante G, Palmieri MB, Esposito G, etal. Apoptotic
cells are present in ischemic zones of deep partialthickness burns. J Burn Care Res. 2006;27:688–93.
10. Gravante G, Palmieri MB, Delogu D, Montone
A. Apoptotic cells in cutaneous adnexa of burned
patients. Burns. 2007;33:129–30.
11. Gravante G, Palmieri MB, Esposito G, etal. Apoptotic
death in deep partial thickness burns vs. normal skin
of burned patients. J Surg Res. 2007;141:141–5.
12. Gravante G, Delogu D, Palmieri MB, etal. Inverse
relationship between the apoptotic rate and the time
elapsed from thermal injuries in deep partial thickness
burns. Burns. 2008;34:228–33.
13. Singer AJ, McClain SA, Taira BR, et al. Apoptosis
and necrosis in the ischemic zone adjacent to third
degree burns. Acad Emerg Med. 2008;15:549–54.
14. Giles N, Rea S, Beer T, et al. A peptide inhibitor of c-Jun promotes wound healing in a mouse
full-thickness burn model. Wound Repair Regen.
2008;16:58–64.
15. Chitnis D, Dickerson C, Munster AM, Winchurch
RA. Inhibition of apoptosis in polymorphonuclear
neutrophils from burn patients. J Leukoc Biol.
1996;59:835–9.
16. Parihar A, Parihar MS, Milner S, Bhat S.Oxidative
stress and anti-oxidative mobilization in burn injury.
Burns. 2008;34:6–17.
17. Ogura H, Hashiguchi N, Tanaka H, etal. Long-term
enhanced expression of heat shock proteins and
decelerated apoptosis in polymorphonuclear leukocytes from major burn patients. J Burn Care Rehabil.
2002;23:103–9.
18. Hirche C, Hrabowski M, Kolios L, etal. Emergency
prehospital care of burn injuries: thermal, electrical
and chemical burns. J Paramed Prat. 2011;3:10–8.
19. Krämer PF, Grützner PA, Wöl CG.Care of burn victims. Preclinical management. Notfall Rettungsmed.
2010;13:23–30.
20. Allison K, Porter K. Consensus on the pre-hospital
approach to burns patient management. J R Army
Med Corps. 2004;150:10–3.
21. Lonnecker S, Schoder V. [Hypothermia in patients
with burn injuries: inuence of prehospital treatment].
Chirurg. 2001;72:164–7.
22. Ipaktchi K, Mattar A, Niederbichler AD, et al.
Attenuating burn wound inammatory signaling
reduces systemic inammation and acute lung injury.
J Immunol. 2006;177:8065–71.
86
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licensed material. You do not have permission under this license to share adapted material derived from this chapter or
parts of it.
The images or other third party material in this chapter are included in the chapter's Creative Commons license,
unless indicated otherwise in a credit line to the material. If material is not included in the chapter's Creative Commons
license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to
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C. Hirche et al.
Electrical Burns
ChristianHerlin
11
11.1 Introduction
Electrical burns are rare but can be particularly
severe or injuring and sometimes fatal. They represent approximately 5% of burns [1]. In addition, it is estimated that 4000 people every year
undergo an electrocution in France.
This type of burn affects mainly two catego-
ries of patients:
• The young child exploring his environment.
• The adult in his workplace.
They are of two types:
• Damage by direct contact with the electric
current. The lesions spreading from an entry
point to an exit point of the current (our focus
of interest in this chapter).
• Injury by electric arcs in accidents at very high
voltage. That is mainly thermal burns but at a
very high temperature (>2000°C).
They can be divided into two groups:
• Low-voltage injuries (<1000 V) occurring
mainly at home.
• High-voltage injuries (>1000 V) occurring
more often in the workplace.
In a recent review of the literature [2] 44% of
patients presented low-voltage injuries (LVIs)
and 38.3% high-voltage injuries (HVIs), and
some studies did not characterise outcomes
according to LVIs vs. HVIs. Psychological outcomes such as post-traumatic stress disorder
were poorly documented. Mortality rates from
electrical injuries are 2.6% in LVI, 5.2% in HVI,
and 3.7% in not otherwise specied situations
with a ratio of 2.4:1 for deaths caused by LVI
compared with HVI.HVIs lead to greater morbidity and mortality than LVIs. However, the
results may suggest that immediate mortality
from LVI may be underestimated.
They mainly concern two locations:
• The upper limb.
• The face.
Mechanisms of tissular injury appear to be of
three different types:
• The Joule effect: generating heat depending
C. Herlin (*)
Wound Healing Unit, Department of Surgery,
Montpellier University, Montpellier, France
e-mail: c-herlin@chu-montpellier.fr
© The Author(s) 2024
L. Téot et al. (eds.), Skin Necrosis, https://doi.org/10.1007/978-3-031-60954-1_11
on tissue resistance—“J=R I2 T.” The amount
of the heat intensity generated (J) depends
indeed on voltage U because U=RI. T is the
87
88
C. Herlin
duration in seconds of the contact, R is the
resistance in ohms, and I is the intensity in
amperes.
• The higher the resistance, the greater the heat
generated will be and the more serious the
injuries are, but less current will travel
through.
• Actually, two parameters inuence tissue
resistance:
• Its category (with decreasing resistance):
Bone>fat> skin > muscle > mucosa > vessel>nerve.
• Its diameter: the smaller the diameter (wrist,
elbow, and ankle), the higher the resistance,
and thus the damage related to the Joule effect
is signicant [2].
• Cell membrane destruction by electric shock
(electroporation) [3] increasing tissue damage
and promoting the release of myoglobin.
• Massive depolarisation, which will result in the
damage of muscle and cardiac and nervous cells.
The “shock” causes the phenomenon of tetanisation, which increases the contact time of the victim with the electric current source (cable grasps,
feeling of being “stuck” to the source).
Furthermore, tetanisation allows the joint’s jump
of current by hyperexion of the joints [4].
11.2 Tissue Injury
11.2.1 Entry andExit Skin Points
These points are most often located at the extremities. The entry point is centred by a sore indicating carbonisation. This area is surrounded by a
burn of decreasing depth (“cockade aspect”). On
the way to the exit point, an area of deep burn
should be suspected, following theoretically the
path of sensory and motor nerves (the supercial
veins also).
However, the current path remains unpredictable. Meanwhile, the exit point more often represents a whitish area. During the impact, it links
the body to the ground or other external elements
connected to it (Fig.11.1).
11.2.2 Muscle Injury
It is always more severe than suggested by skin
lesions and is due to the action of depolarisation
and Joule effect. It represents the most important
vital and functional prognosis factor in this type
of burn. Muscles submitted to high voltage will
undergo a very signicant oedema, which can
Fig. 11.1 Example of multiple points of entry and exits in the same patient
11 Electrical Burns
Fig. 11.2 Carbonisation of upper limb responsible for
major and composite tissue lesions
89
of a shaper must be compulsory if there is a risk
of microstomia.
11.2.5 Nerve Damage
It is most often a direct injury of axons by the
current, causing paralysis or sensory disturbances
more or less permanent. Indirect injury, often
persistent, is caused by thrombosis or
compression.
lead quickly to a compartment syndrome
(>30mmHg). This syndrome, if not managed by
a fasciotomy, will signicantly increase muscle,
nerve, and vascular damage, by direct compression, thrombosis [5], and necrosis, leading to
local acidosis. This vicious cycle is to be broken
as soon as possible (Fig.11.2).
11.2.3 Myocardial Damage
Except the acute cardiac brillation, approximately 10% of patients admitted for electrical
burn present electrocardiographic abnormality.
This is most often represented by bundle branch
block, supraventricular tachycardia, or nonspecic repolarisation disorder. To these mechanisms is added necrosis by coronary thrombosis
according to the same mechanisms mentioned
above.
11.2.4 Buccal Mucosa Damage
11.2.6 Deep Damage (Except Viscera)
They are the consequences of the Joule effect.
With the bone and fascia being poor conductors,
the heat effect is very signicant, causing periosteal bone necrosis. In addition to that, fractures
and serious sprains (typical posterior
glenohumeral dislocation) are not uncommon
due to tonic muscle tetanisation.
11.2.7 Other Damages
• Renal: damage by renal parenchymal necro-
sis, thrombosis, or disseminated intravascular
coagulation (DIC) and acute tubular necrosis
by accumulation of myoglobin.
• Visceral damage represented by gastrointesti-
nal perforation, paralytic ileus, hepatorenal
syndrome, liver injury, or acute pancreatitis.
Liver enzymes as well as amylase/lipase are to
be obtained.
It is typical of young children biting electric
cables. The lesions are most often at the commissures, gums, and tongue. Full necrosis occurs
most often before the end of the second week.
Spontaneous wound healing is often adequate,
but sometimes secondary interventions are
required [6]. Their objective is in fact to reconstruct the anatomical subunits. The establishment
11.3 Medical Management
11.3.1 Monitoring
The intensive care management (cardiovascular
monitoring, rehydration, coagulation, CPK, K+,
etc.) must be rigorous and precautionary [7].
Compartment syndrome is to be ruled out
90
C. Herlin
(increased pressure of the compartments, hypoaesthesia, impaired distal perfusion, etc.).
11.3.2 Assessment oftheLesions
If entry and exit skin points are usually obvious,
the path and the internal damages are sometimes
more difcult to assess. Scintigraphy (99mTc;
133X) and MRI can provide important information on the condition about the deep integuments
[8].
11.4 Surgical Management
11.4.1 First Surgery
It must be determined by the existence of a compartment syndrome, which must be managed
within 6h of the injury [9]. Deep exploration is to
be done while carrying out escharotomies and
fasciotomies. Necrotic tissue should be removed;
the damaged muscles and nerves have to be preserved if we consider a possible recovery especially after fasciotomy (Fig.11.3).
Immediate ap coverage is recommended by
many authors to limit devascularisation, but in
emergency cases, we think that it must be
reserved for vital organ coverage [10]. Besides
these situations, we believe that we must avoid
performing locoregional or free aps before
3weeks to allow time for oedema to decrease and
promote drainage of all local toxins (free radicals, lactate) leached after the trauma. Immediate
amputation is limited to extreme cases with
anuria or shock; it will aim to keep a length
always compatible with future equipment.
11.4.2 Second Look
It is carried out 2–3days later. We have to spare
the maximum of tissue (tendon, nerve, etc.) even
if they fall in a grey zone. Skin coverage remains
our priority; the damaged nerves will be repaired
in a second time. Even if not widely practised,
these interventions bring some interest as they
will allow being less aggressive in the rst surgery and opening a window for a new debridement of secondary necrotic tissue after the
removal of the ischemia-reperfusion syndrome
Fig. 11.3 Deep burn of the lateral side of the face due to a very-high-voltage electric arc
11 Electrical Burns
91
Fig. 11.4 Realisation of an island ap for the reconstruction of the proximal defect. Skin graft was used for the middle
nger
(when fasciotomy is performed). Ultimately, a
third or a fourth revision is sometimes necessary
to achieve complete debridement of large areas
(Fig.11.4).
Furthermore, a polymicrobial infection of
necrotic tissue can occur with plurimicrobiens
processes often including anaerobes or
Pseudomonas aeruginosa. Bacteriological sam-
It is indeed known that electrocution can have
a psychological impact and even cause psychiatric diseases.
The nal healing is often long and delayed.
Thus, 3–4weeks may be required to obtain granulation tissue after debridement and 2–3months
to hope for healing of the entry and exit skin
points.
ples are systematically taken, and antibiotics are
given as needed.
11.6 Prevention
11.5 Global Management
This type of patients requires hospitalisation in
specialised burn unit with experienced teams.
Supervision by physiotherapists to limit retractions is necessary, but also the psychological side
should not be neglected.
In developed countries, electrical burns occurring
in working conditions as well as paediatric burns
have decreased, and most of the patients are
admitted with low-voltage burns, whereas in
developing countries, patients are more frequently admitted with high-voltage burns, with
an extensive need for acute and reconstructive
92
C. Herlin
surgical interventions. Voltage of the burn injury
is a determinant factor in the severity of the
necrotic lesions. A reduction in paediatric highvoltage injuries was observed over the past two
decades, likely due to the enhancement of electrical safety [11, 12].
11.7 Conclusion
The electrical burns are rare but often severe. The
initial management is dominated by the detection
of deep lesions and the prevention of organ failure. Management of muscle injury is important
for vital and functional outcomes; however, it
remains very difcult to assess in the early days.
Surgery is often delayed and should usually aim,
after a second look, to restore the original anatomy and function. Cosmetic and functional
sequelae will be supported later, usually at
18–24months.
References
1. Koumbourlis AC. Electrical injuries. Crit Care
Med. 2002;30(11 Suppl):S424–30. PubMed PMID:
12528784
2. Shih JG, Shahrokhi S, Jeschke MG.Review of adult
electrical burn injury outcomes worldwide: an analysis of low-voltage vs high-voltage electrical injury. J
Burn Care Res. 2017;38(1):e293–8.
3. Hunt JL. Electrical injuries of the upper extremity.
Major Probl Clin Surg. 1976;19:72–83. PubMed
PMID: 1256066
4. Lee RC, Gaylor DC, Bhatt D, Israel DA.Role of cell
membrane rupture in the pathogenesis of electrical
trauma. J Surg Res. 1988;44(6):709–19. PubMed
PMID: 3379948
5. Skoog T. Electrical injuries. J Trauma.
1970;10(10):816–30. PubMed PMID: 5506363
6. Holliman CJ, Safe JR, Kravitz M, Warden GD.Early
surgical decompression in the management of electrical injuries. Am J Surg. 1982;144(6):733–9. PubMed
PMID: 7149133
7. Garson S.Les levres brulees [Burned lips]. Ann Chir
Plast Esthet. 2002;47(5):547–55. PubMed PMID:
12449878
8. Purdue GF, Hunt JL.Electrocardiographic monitoring
after electrical injury: necessity or luxury. J Trauma.
1986;26(2):166–7. PubMed PMID: 3944840
9. Ligen L, Hongming Y, Feng L, Huinan Y, Quan H,
Guang F. Magnetic resonance imaging features of
soft tissue and vascular injuries after high-voltage
electrical burns and their clinical application. Injury.
2012;43(9):1445–50. PubMed PMID: 21764053
10. Teot L, Griffe O, Brabet M, Gavroy JP, Thaury
M.Severe electric injuries of the hand and forearm.
Ann Hand Upper Limb Surg. 1992;11(3):207–16.
PubMed PMID: 1382511
11. Zhu ZX, Xu XG, Li WP, Wang DX, Zhang LY,
Chen LY, et al. Experience of 14 years of emergency reconstruction of electrical injuries. Burns.
2003;29(1):65–72. PubMed PMID: 12543048
12. Depamphilis MA, Cauley RP, Sadeq F, Lydon M,
Sheridan RL, Driscoll DN, Winograd JM. Surgical
management and epidemiological trends of pediatric
electrical burns. Burns. 2020;46(7):1693–9. https://
doi.org/10.1016/j.burns.2020.03.005. Epub 2020 Mar
31.PMID: 32245570
Open Access This chapter is licensed under the terms of the Creative Commons Attribution-NonCommercialNoDerivatives 4.0 International License (http://creativecommons.org/licenses/by- nc- nd/4.0/), which permits any noncommercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit
to the original author(s) and the source, provide a link to the Creative Commons license and indicate if you modied the
licensed material. You do not have permission under this license to share adapted material derived from this chapter or
parts of it.
The images or other third party material in this chapter are included in the chapter's Creative Commons license,
unless indicated otherwise in a credit line to the material. If material is not included in the chapter's Creative Commons
license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to
obtain permission directly from the copyright holder.
Gunshot Wounds
SupapornOpasanon
andApiragChuangsuwanich
12
12.1 Introduction
Gunshot wounds (GSWs) are one of the most
fatal traumatic injuries. Bullets not only cause
direct vital organ damage, but also further
problems from undermanagement of the
wounds [1–3]. Soft tissue damage, foreign
bodies, and bacterial contamination at GSW
sites and along the wound tract are the factors
that may cause infection and delay wound
healing [4, 5]. After the Advanced Trauma Life
Support (ATLS®) protocol [2] for life-threatening condition, GSWs should be managed thoroughly. In this chapter, we describe the updated
knowledge and principle of GSW
management.
12.2 Etiopathogeny
Gunshot causes tissue damages by disrupting
the tissue, through bleeding, and by permitting
entrance of infection [1–3, 6]. The mechanism
of tissue injuries is mixed, blunt, and penetrating trauma injuries. For penetrating trauma,
S. Opasanon
Faculty of Medicine, Division of Trauma Surgery,
Department of Surgery, Siriraj Hospital, Mahidol
University, Bangkok, Thailand
A. Chuangsuwanich (*)
Faculty of Medicine, Division of Plastic Surgery,
Department of Surgery, Siriraj Hospital, Mahidol
University, Bangkok, Thailand
destruction of esh tissue is due to passing of
the bullet through it and the large amount of
kinetic energy transferred to the tissue. Some
blunt trauma is due to displacement of tissue
adjacent to the track of the penetrating bullet.
The bullet’s shock wave may damage the adjacent structure. Severity of a bullet wound may
be expressed by the formula KE=½ MV2. This
formula expresses the amount of the energy
transfer to the body by a bullet. Contusion and
hemorrhage will occur. Increasing the velocity
of the bullet will have more tissue destruction
than increasing its mass. A bullet is not sterilized and may carry viable bacteria and clothing
into a wound [4, 5].
12.3 Clinical Detailing
12.3.1 Characteristics ofGSWs
Tissue destruction relies on the kinetic energy of
the bullet. A high-velocity bullet causes more tissue damage than a low-velocity bullet. The anatomy of the wounds is also an important factor of
severity:
© The Author(s) 2024
L. Téot et al. (eds.), Skin Necrosis, https://doi.org/10.1007/978-3-031-60954-1_12
93